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Many different mechanisms are involved in thrombus formation. We compared the effects on haemostatic function of two drugs having different mechanism of action, the one interfering with arachidonic acid metabolic cascade (Indobufen) and the other (Ticlopidine) independent from it. 18 adult patients of both sexes suffering from cerebral Transient Ischaemic Attack (T.I.A.) or Reversible Ischaemic Neurologic Disability (R.I.N.D.) have been treated with Indobufen (400 mg daily) or Ticlopidine (500 mg daily) for three weeks. The effects on various haemostatic parameters including bleeding time, platelet adhesion to glass beads, platelet aggregation induced by ADP, collagen, platelet activating factor (PAF )f have been evaluated at the beginning and at the end of treatment. Both drugs prolonged the bleeding time, Ticlopidine being more effective than Indobufen. ADP-induced platelet aggregation was more effectively inhibited by Ticlopidine, while Indobufen was more effective on collagen-induced aggregation. PAF-induced platelet aggregation was inhibited by Ticlopidine, while Indobufen was ineffective. Platelet adhesion to glass beads was not influenced by treatment with either drugs. In conclusion, both drugs confirmed to be effective in inhibiting haemostatic function although with different mechanisms. Ticlopidine seems to be involved in more mechanisms, interfering with platelet aggregation induced by ADP, collagen, PAF and prolonging the bleeding time. Indobufen interferes with platelet aggregation induced by ADP and collagen, is less effective in prolonging the bleeding time, and does not affect PAF-induced platelet aggregation.

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